CTRP3 exacerbates tendinopathy by dysregulating tendon stem cell differentiation and altering extracellular matrix...

Area of Science:

• Biochemistry
• Molecular Biology
• Orthopedics

Background:

• Tendinopathy is a prevalent tendon disorder marked by matrix disorganization, often leading to tears and rupture.
• Identifying specific molecular targets is crucial for developing effective therapeutic interventions for tendinopathy.

Purpose of the Study:

• To identify a molecular target for therapeutic intervention in tendinopathy.
• To investigate the role of C1q/TNF-related protein-3 (CTRP3) in tendinopathy pathogenesis.

Main Methods:

• Identified CTRP3 as upregulated in human and rodent tendinopathy models.
• Utilized CTRP3 overexpression and knockdown in mouse tendons.
• Administered a neutralizing antibody against CTRP3 to treat overuse-induced tendinopathy.

Main Results:

• CTRP3 overexpression exacerbated tendinopathy, increasing proteoglycans and degenerating collagen.
• CTRP3 knockdown suppressed tendinopathy progression.
• Antibody blockade of CTRP3 ameliorated Achilles and rotator cuff tendinopathy.
• CTRP3 promoted abnormal stem cell differentiation and chondrification via Akt signaling.

Conclusions:

• CTRP3 plays a critical role in the pathogenesis of tendinopathy.
• Functional blockade of CTRP3 presents a promising therapeutic strategy for treating tendinopathy.